Aortic prostacyclin release is lowered by superior mesenteric artery occlusion (SMAO) shock in pigs.

We have previously demonstrated altered platelet reactivity subsequent to splanchnic artery occlusion (SAO) shock in pigs: decreased reactivity, such as might be seen subsequent to submaximal stimulation, was observed in the postrelease period. Prostacyclin (PGI2) formed and released by vessel endothelium may function as a circulating hormone and regulate platelet reactivity by opposing the stimulatory influence of other factors. We have therefore investigated PGI2 release by aortas taken at "death" (systolic blood pressure = 30 mmHg) from pigs subjected to shock induced by a 2-hr occlusion of the superior mesenteric artery (SMAO). This shock is analogous to, but with a longer time course than, SAO shock. Aortas from sham-operated animals (matched for "death" time to the SMAO animals) served as controls. Thoracic aortas were removed, placed in cold 50 mM pH 7.5 tris buffer, cleaned of adhering tissue or clots, cut into rings and suspended in room temperature 50 mM pH 7.5 tris buffer into which PGI2 was released. Aliquots of the latter were quantitated for PGI2 by bioassay using human platelets for which a dose-response relationship for pure, synthetic PGI2 had been established: aliquot PGI2 quantities were determined graphically from the log dose-response (percentage inhibition of aggregation) curves, and converted arithmetically to amount per weight tissue. After 10 min incubation of tissue in buffer, the mean +/- SEM PGI2 for the shock animals (N = 8) was 0.053 +/- 0.02 ng/mg, and for the sham animals (N = 7), 0.174 +/- .06; the P value for t-test of means was 0.083. For 30-min incubation, the mean PGI2 for the shock group was 0.052 +/- 0.02 and for the sham, 0.283 +/- 0.11; the P value was 0.029. Inhibitory activity of the buffer aliquots declined in parallel with authentic PGI2. Thus, the occurrence of SMAO shock resulted in a significant decrease in aortic release of PGI2. Altered platelet reactivity as a consequence of shock, such as demonstrated by us and by others, could thus be in part a result of lowered endothelial release of PGI2, either alone or in combination with the occurrence of activation by other factors.